Rheumatoid Arthritis
Left ventricular structure and function in patients with rheumatoid arthritis, as assessed by cardiac magnetic resonance imaging
Article first published online: 28 JAN 2010
DOI: 10.1002/art.27349
Copyright © 2010 by the American College of Rheumatology
Additional Information
How to Cite
Giles, J. T., Malayeri, A. A., Fernandes, V., Post, W., Blumenthal, R. S., Bluemke, D., Vogel-Claussen, J., Szklo, M., Petri, M., Gelber, A. C., Brumback, L., Lima, J. and Bathon, J. M. (2010), Left ventricular structure and function in patients with rheumatoid arthritis, as assessed by cardiac magnetic resonance imaging. Arthritis & Rheumatism, 62: 940–951. doi: 10.1002/art.27349
Publication History
- Issue published online: 30 MAR 2010
- Article first published online: 28 JAN 2010
- Accepted manuscript online: 28 JAN 2010 12:00AM EST
- Manuscript Accepted: 21 DEC 2009
- Manuscript Received: 8 JUL 2009
Funded by
- NIH (National Institute of Arthritis and Musculoskeletal and Skin Diseases). Grant Number: AR-050026
- National Heart, Lung, and Blood Institute. Grant Numbers: N01-HC-95159, N01-HC-95166, N01-HC-95169
- Arthritis National Research Foundation
- Abstract
- Article
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- Cited By
Abstract
Objective
Heart failure is a major contributor to cardiovascular morbidity and mortality in patients with rheumatoid arthritis (RA), but little is known about myocardial structure and function in this population. This study was undertaken to assess the factors associated with progression to heart failure in patients with RA.
Methods
With the use of cardiac magnetic resonance imaging, measures of myocardial structure and function were assessed in men and women with RA enrolled in the Evaluation of Subclinical Cardiovascular Disease and Predictors of Events in Rheumatoid Arthritis study, a cohort study of subclinical cardiovascular disease in patients with RA, in comparison with non-RA control subjects from a cohort enrolled in the Baltimore Multi-Ethnic Study of Atherosclerosis.
Results
Measures of myocardial structure and function were compared between 75 patients with RA and 225 frequency-matched controls. After adjustment for confounders, the mean left ventricular mass was found to be 26 gm lower in patients with RA compared with controls (P < 0.001), an 18% difference. In addition, the mean left ventricular ejection fraction, cardiac output, and stroke volume were modestly lower in the RA group compared with controls. The mean left ventricular end systolic and end diastolic volumes did not differ between the groups. In patients with RA, higher levels of anti–cyclic citrullinated peptide (anti-CCP) antibodies and current use of biologic agents, but not other measures of disease activity or severity, were associated with significantly lower adjusted mean values for the left ventricular mass, end diastolic volume, and stroke volume, but not with ejection fraction. The combined associations of anti-CCP antibody level and biologic agent use with myocardial measures were additive, without evidence of interaction.
Conclusion
These findings suggest that the progression to heart failure in RA may occur through reduced myocardial mass rather than hypertrophy. Both modifiable and nonmodifiable factors may contribute to lower levels of left ventricular mass and volume.

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